2in the sheets give rise to osteoblasts, which rapidly deposit spongy bone with trabeculae of woven bone(collagen fibers randomly arranged; no lamellea)between them

(intramembranous ossificaion) connective tissue becomes?

3periosteum

(intramembranous ossification)woven bone is replaced by

4lamellar bone(collagen fibers arranged in parallel within lamellae)

(intramembranous ossification)where do compact and spongy bone mature

5lamellar

(intramembranous ossification)how do layers of spongy bone matrix become compact

6by filling in spaces with bony matrix

(endochondral ossification) mostt bones develop from

hyaline cartilage model

(endochondral ossification)what does perichondrium become?

1periosteum; its osteoblasts produce a bony collar of compact bone around the model,causing deposition of calcium phosphate in extracellular matrix(calcification of cartilage),cutting off nutrition to the chondrocytes

(endochondral ossification)what happens to chonrocytes when they die

2their lacunae enlarge

(endochondral ossification)what happens at the primary(diaphysis and secondary(epiphyses)ossification centers?

3vascular buds from the periosteum break down the cartilaginous lacunae,forming marrow cavity(in diaphysis)

movement of molecules of any substance to spread evenly into available space due to random thermal motion of molecules occurs along concentration gradient of diffusing substance does not require expenditure of energy

a cell that does not differentiate or divide undergoes apoptosis(programmed cell dealth)

apoptosis sculpts organs during development causes uterus to shrink after childbirth ,peels away damaged skin after sunburn;synchronized with mitosis

cell death(death receptor and enzymes)

death receptor on doomed cells membrane receives signal to die,activates caspases(enzymes) destroy enzymes that replicate &repair dna,activate enzymes that cut up dna,fracture mitrochondria,abolish the cells ability to adhere to other cells

any mutation that decreases normal activity of a tumor suppressor gene may contribute to the onset of cancer

cancer cells

do not respond to normal signals that regulate the cell cycle

divide excessively&invade other tissues

kill the organism if unchecked

lack of density-dependent inhibition&anchorage dependence

do not require growth factors to divide

stop dividing at random points in cell cycle

can go on dividing indefinitely because of high levels of telomerase

transformation

conversion of a normal cell to a cancer cell,more tham 1 somatic cell mutation is generally needed to produce full fledged cancer including appearance of at least one oncogene&loss of several tumor suppressor genes,bodys immune system destroys tranformed cells,surviving transformed cells proliferate,forming tumor

tumor

mass of abnormal cells remain at the orgiginal site;can be completly removed by surgery

Line cavities &tubes that open to the outside composed of nonkeratinized stratified squamous or pseudo stratified or simple columnar epithelium&layer of areolar tissue goblet cells in the epithelial umm secret mucus

serous membranes

line body cavities that do not open 2 the outside&reduce friction between organs&cavity walls,viseral membrane covers the internal organ,parietal membrane lines the body cavity,made of simple squamous epithelium& a thin layer of areolar tissue,cells secrete lubricating serous fluid